Background: Periodontitis has been described as a chronic inflammatory disease which is triggered by specific host dependent immune response. It is established that the immune response is influenced among others by a genetic predisposition. In recent times it was shown, that the gene expression is affected also by epigenetic modifications. Therefore, we investigated the CpG methylation pattern of 22 inflammatory candidate genes (ATF2, CCL25, CXCL14, CXCL3, CXCL5, CXCL6, FADD, GATA3, IL10RA, IL12A, IL12B, IL13, IL13RA1, IL15, IL17C, IL17RA, IL4R, IL6R, IL6ST, IL7, INHA, TYK2) in dependence of the periodontal status.Patients and methods: In this preliminary study 11 patients with aggressive periodontitis (54.5% males, 40.6+11.5years) and 10 periodontal healthy persons (40% males, 37.7+17.1years) were included. Gingival biopsies were obtained and immediately frozen in liquid nitrogen. After DNA isolation (QIAamp® DNA Micro Kit) the methylation pattern was quantified using EpiTect® Methyl II Signature PCR Array Human Inflammatory Response (Qiagen). Results: In gingival inflamed tissues of patients with aggressive periodontitis there was a significant reduction in CpG methylation pattern of interleukin 17C compared with tissues of periodontal healthy persons (6.1% vs. 26.4%, p=0.007). The methylation pattern of all other genes investigated was not significantly modified regarding periodontal inflammation.Discussion: In our study we show for the first time a differential methylation pattern for IL17C in periodontitis. Interleukin 17C is an essential autocrine cytokine that regulates innate epithelial immune responses induced by bacterial challenge and inflammatory stimuli. The decrease in CpG methylation is presumably accompanied by an increase in gene expression. This could lead to a greater availability of interleukin 17C and the induction of epithelial immune response in inflamed oral tissue.